These high energy devices include a pulse generator which monitors the cardiac activity in both the atrial and the ventricular cardiac chambers and generates pulses of stimulation energy (a "stimulation" pulse) or high energy (a "shock" pulse) when the heart presents a ventricular arrhythmia susceptible to be treated. When the shock pulse energy is between 0.1 and 10 J approximately, one designates this therapy under the name of "cardioversion" and the electrical shock is called a "cardioversion shock". When the shock pulse energy is greater than 10 J approximately, the therapy is called defibrillation and the electrical shock is called a "defibrillation shock".
This shock pulse therapy is desired to be delivered when one detects a ventricular tachycardia (VT), but only in the case that the detected tachycardia is a real VT, and not a supra-ventricular tachycardia (SVT). Indeed, in the latter case, the tachycardia is of atrial origin and the high energy shock pulse that would be delivered would not have any effect because the defibrillation electrode or, if appropriate, the stimulation electrode, is not found in the atrial region.
A tachyarrythmia (also known as a tachycardia) corresponds to an abnormal rapid cardiac rhythm, and includes ventricular fibrillation (VF), ventricular tachycardia (VT), sinus tachycardia (ST), and supra-ventricular tachycardia (SVT). The supra-ventricular tachycardia (SVT) includes atrial tachycardia (AT), atrial flutter and atrial fibrillation (AF).
The diagnosis of tachycardias can be performed, in any manner that is known (see for example, EP-A-0 626 182 and its corresponding U.S. Pat. No. 5,462,060, commonly assigned to ELA Medical, which U.S. Pat. No. 5,462,060 is incorporated herein by reference in its entirety), from criteria such as the ventricular frequency, the ventricular interval stability (the RR interval), the analysis of the atrial-ventricular association (as made be revealed by the stability of the PR interval) and the mode of beginning of the tachycardia (that is, the presence of an abrupt or rapid acceleration and the cavity of origin, ventricular or atrial).
More precisely, the device described in the aforementioned EP and U.S. patents defines that there is stability of the RR intervals when the peak of auto-correlation, divided by the total of auto-correlation, exceeds a determined ratio (the peak of auto-correlation is the maximal number of recent intervals in the ventricle that satisfying a predetermined stability criterion).
It also defines that there is conduction stability when the value of the peak of cross-correlation is divided by the value of the peak of auto-correlation (or, in an other embodiment by the total of cross-correlation) exceeds a determined reference (the peak of cross-correlation is the maximal number of intervals of conduction from the atrium that satisfy a predetermined stability criterion). In others words, in the first aforementioned case, one compares the stability of the conduction between the two cavities to those of intervals in the ventricle, while in the second case one expresses the stability of the conduction between the two cavities according to the presumed totality of conduction.
When there is no stability in the ventricle (that is, there are unstable RR intervals), that means that the tachyarrythmia is probably not susceptible to be interrupted by a therapy applied to the ventricle, and the process then determines that it is not susceptible to be interrupted in this cavity.
On the other hand, when there is stability in the ventricle (i.e., stable RR intervals), but not stability of conduction (i.e., an absence of atrial-ventricular association), that means that the tachyarrythmia probably has its origin in the ventricle, and the process determines that it is susceptible to be interrupted by a shock therapy applied to the ventricle.
Whenever there is stability in the ventricle (stable RR intervals), and also a conduction stability (established atrial-ventricular association), the process in question determines if the conduction from the second cavity is 1:1 or n:1. This is done by comparing the peak of cross-correlation to the total of cross-correlation. In the case of a 1:1 association, one considers another criterion, namely the presence or absence of an acceleration (rapid acceleration) originating with a dissociation, to determine whether or not the tachyarrythmia is susceptible to be interrupted by stimulation pulses and/or electrical shock pulses (cardioversion or defibrillation).
In the case of a n:1 association, one concludes that the tachyarrythmia is in no manner susceptible to be interrupted by stimulation of the ventricle, because the tachyarrythmia has its origin in the atrium.
One observes, however, in some cases, a clinical failure of the foregoing classification algorithm.
French patent application No. 96 07533 and its corresponding U.S. application Ser. No. 08/877039 filed Jun. 17, 1997, commonly assigned to the assignee hereof, ELA Medical, which US application is incorporated herein by reference in its entirety, described in this regard an improvement that allows one to detect the presence of long RR cycles so as to insure a supplementary discrimination between VT and SVT, especially in the presence an installed and conducted AF presenting regular RR intervals during a sufficiently long duration, to conclude a false diagnosis of VT (regular rhythm and dissociation between atrium and ventricle). However, the clinical observation reveals that, in some cases of tachyarrhythmias really necessitating a therapy, this therapy has not been applied, or it has been applied too late. These particular cases will now be explained with reference to FIGS. 1 to 3, that represents the evolution of the value of the RR intervals (a "short" RR interval corresponds to a high ventricular rhythm) over the course of a succession of such cycles.
In the case illustrated in FIG. 1, the RR intervals rapidly become very stable, with a typical difference of 63 ms between the minimal value and the maximal value for the seventeen cycles preceding the shock therapy, which is applied on the n.sup.th cycle 95. The algorithm has indeed interpreted this situation as corresponding to a stability of RR intervals with an absence of association, resulting in a diagnosis of VT, which is normally susceptible to shock therapy.
Nevertheless, the presence of a long RR cycle at 10 indicates, in a manner clear to the clinician, that it does not concern a VT, but rather an SVT, which is not reducible by a shock therapy. One sees, in this example, that the classification of the prior art device has produced a false positive diagnosis (an indication of a VT, although it actually concerned an SVT).
In the cases of FIGS. 2 and 3, conversely, a progressive variation of the RR interval (at 20 on FIG. 2), or an instability of the RR interval over very short cycles (at 30 on FIG. 3), has been interpreted by the classification of the prior art device as an instability of the RR rhythm, thus concluding wrongly at 50 that it was not necessary to apply a therapy. In these examples, the criterion to diagnose and process a VT was the detection of at least six cycles in the peak of autocorrelation (defining the RR interval stability) during eight continuous cycles while, in the cases of FIGS. 2 and 3, the duration of persistence of the RR stability had not exceeded five and six cycles, respectively.
In these two latter examples, one has therefore reached a false negative diagnosis, that is to say the device classification concluded an SVT existed although it really concerned a VT.